Family matters: How MYC family oncogenes impact small cell lung cancer

被引：70

作者：

Braegelmann, Johannes ^{[1
,2
]}

Boehm, Stefanie ^{[1
,2
]}

Guthrie, Matthew R. ^{[3
]}

Mollaoglu, Gurkan ^{[3
]}

Oliver, Trudy G. ^{[3
]}

Sos, Martin L. ^{[1
,2
,4
]}

机构：

[1] Univ Cologne, Inst Pathol, Mol Pathol, D-50937 Cologne, Germany

[2] Univ Cologne, Med Fac, Dept Translat Genom, Cologne, Germany

[3] Univ Utah, Huntsman Canc Inst, Dept Oncol Sci, Salt Lake City, UT 84112 USA

[4] Univ Cologne, Ctr Mol Med Cologne, Cologne, Germany

来源：

CELL CYCLE | 2017年 / 16卷 / 16期

关键词：

MYC; MYCL; MYCN; small cell lung cancer; SCLC; GEMM; mouse models; SMALL-MOLECULE INHIBITORS; MESSENGER-RNA STABILITY; RIBOSOMAL-PROTEIN L11; DNA-DAMAGE RESPONSE; C-MYC; N-MYC; AURORA KINASE; NEUROENDOCRINE TUMORS; GENE-EXPRESSION; MOUSE MODELS;

D O I：

10.1080/15384101.2017.1339849

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Small cell lung cancer (SCLC) is one of the most deadly cancers and currently lacks effective targeted treatment options. Recent advances in the molecular characterization of SCLC has provided novel insight into the biology of this disease and raises hope for a paradigm shift in the treatment of SCLC. We and others have identified activation of MYC as a driver of susceptibility to Aurora kinase inhibition in SCLC cells and tumors that translates into a therapeutic option for the targeted treatment of MYC-driven SCLC. While MYC shares major features with its paralogs MYCN and MYCL, the sensitivity to Aurora kinase inhibitors is unique for MYC-driven SCLC. In this review, we will compare the distinct molecular features of the 3 MYC family members and address the potential implications for targeted therapy of SCLC.

引用

页码：1489 / 1498

页数：10

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